Congestive Heart Failure
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Congestive heart failure (CHF) is a pathophysiological syndrome in which the heart is unable to pump an adequate amount of blood to meet metabolic demands. In addition to inadequate cardiac output (CO), there is an elevation of pressure in the left ventricle caused by left ventricular dysfunction. Pressures are reflected backward through the pulmonary veins, causing increased pulmonary pressure and congestion.
Congestive heart failure (CHF) refers primarily to left ventricular failure (LVF). However, the increased pulmonary pressure resulting from LVF increases pressure against which the right ventricle must pump, eventually resulting in right ventricular failure (RVF). The right ventricle is unable to compensate for this increased workload and becomes hypertrophic, leading to failure. Pressures in the systemic venous circulation rise, leading to peripheral edema and hepatosplenomegaly. LVF is the most common cause of RVF. Pulmonary disease, such as chronic obstructive pulmonary disease, cystic fibrosis, or adult respiratory distress syndrome, may also contribute to RVF.
LVF is the most common cause of RVF. Pulmonary disease, such as chronic obstructive pulmonary disease, cystic fibrosis, or adult respiratory distress syndrome, may also contribute to RVF.
CHF is associated with numerous types of cardiovascular disease, especially hypertension and coronary artery disease. More than half of the deaths from heart disease are due to end-stage CHF. One and a half percent to 2% of the American population is afflicted with CHF. There is a 65% 6-year mortality rate for women and an 80% mortality rate for men. CHF results in 700,000 hospital admissions each year and is the most common admitting diagnosis after age 65. It is associated with extended hospital stays, and the resulting costs for these stays are estimated to be $102 billion a year. Research has demonstrated that better control of CHF can substantially reduce health care expenditures. The prevalence of CHF is expected to continue to rise due to the aging population and because of declines in mortality from other cardiovascular disease. Age is the most common risk factor for CHF.
The causes of CHF may be divided into two subgroups: (1) underlying cardiac diseases and (2) causes that precipitate the onset of CHF in those with underlying cardiac problems. In addition to aging, coronary artery disease, a more common cause in whites, and hypertension, a more common cause in African Americans, are other risk factors. Additional risk factors include cardiomyopathy, diabetes, valvular heart disease, and renal failure. Twenty percent of survivors of myocardial infarction, a common cause of CHF, will be incapacitated by CHF within 6 years. Precipitating causes of decompensation in CHF include anemia, infection, hyperthyroidism, hypothyroidism,
exacerbation of hypertension, dysrhythmias, endocarditis, and hypervolemia. Noncompliance with diet or medications can precipitate CHF episodes.
exacerbation of hypertension, dysrhythmias, endocarditis, and hypervolemia. Noncompliance with diet or medications can precipitate CHF episodes.
PATHOPHYSIOLOGY
CHF results from complex interaction among factors that affect contractility: preload, which is the degree of myocardial stretch just before contraction; afterload, the resistance of ejection of blood from the left ventricle; and the subsequent neurohumoral and hemodynamic compensatory responses from decreased CO. Decreased afterload (or lower aortic pressures) allows quicker contractility of the heart. Higher pressures, or increased afterload, reduce contractility, causing higher workload demands upon the heart.
CO is determined by stroke volume multiplied by heart rate. Stroke volume is determined by preload, contractility, and afterload. An increased preload stretches myocardial fibers, increasing the strength of contraction; however, excessive stretch results in decreased contractility. Increased contractility increases stroke volume, but, if excessive, oxygen demand results in decreased contractility. Any increased afterload decreases stroke volume. Heart rate, which is influenced by the autonomic nervous system, increases the CO until it is excessive (>160 beats/min), in which case the duration of diastole is shortened, reducing ventricular filling and stroke volume.